The joint objective of the proposed studies is to investigate the influence of sleep EEG slow wave activity (SWA) on waking neurobehavioral function. SWA will be manipulated using (I) caffeine and (ii) experimental SWA suppression. Study I will distinguish the influences of caffeine on homeostatic and circadian components of the sleep EEG for the first time. Quantitative sleep EEG spectra will be compared between subjects who received caffeine or placebo in a 28-day forced desynchrony protocol. The hypothesis is that caffeine will suppress sleep SWA. Such suppression may account for observed caffeine-induced increases in daytime sleepiness. Caffeine is the world's most commonly used drug. Thus, its effects on sleep physiology and subsequent waking have potentially enormous health implications. Study II will investigate effects of experimental SWA suppression on waking EEG and working memory. Compared with undisturbed sleep, SWA suppression is hypothesized to impair working memory as measured with the N-back task and to produce waking EEG changes in prefrontal cortex as assessed with EEG source localization. Results will elucidate mechanisms of sleep regulation and their relationship to waking function. Findings may lead to an objective assay of drowsiness for accident prevention and may yield insights into psychiatric disorders associated with reduced sleep SWA.